Report of a Simplified Frailty Score Predictive of Short-Term Postoperative Morbidity and Mortality.

BACKGROUND: Frailty is an objective method of quantifying a patient's fitness for surgery. Its clinical use is limited by the time needed to complete, as well as a lack of evidence-based interventions to improve outcomes in identified frail patients. The purpose of this study was to critically analyze the components of the Fried Frailty Criteria, among other preoperative variables, to create a simplified risk assessment amenable to a busy clinical setting, while maintaining prognostic ability for surgical outcomes. STUDY DESIGN: We performed a prospective evaluation of patients that included the 5-component Fried Frailty Criteria, traditional surgical risk assessments, biochemical laboratory values, and clinical and demographic data. Thirty-day postoperative outcomes were the outcomes of interest. RESULTS: There were 351 consecutive patients undergoing major intra-abdominal operations enrolled. Analysis demonstrated that shrinking and grip strength alone hold the same prognostic information as the full 5-component Fried Frailty Criteria for 30-day morbidity and mortality. The addition of American Society of Anesthesia (ASA) score and serum hemoglobin creates a composite risk score, which facilitates easy classification of patients into discrete low (ref), intermediate (odds ratio [OR] 1.974, 95% CI 1.006 to 3.877, p = 0.048), and high (OR 4.889, 95% CI 2.220 to 10.769, p < 0.001) risk categories, with a corresponding stepwise increase in risk for 30-day postoperative complications. Internal validation by bootstrapping confirmed the results. CONCLUSIONS: This study demonstrated that 2 components of the Fried Frailty Criteria, shrinking and grip strength, hold the same predictive value as the full frailty assessment. When combined with American Society of Anesthesiologists score and serum hemoglobin, they form a straightforward, simple risk classification system with robust prognostic information.

Inhaled prostacyclin is safe, effective, and affordable in patients with pulmonary hypertension, right heart dysfunction, and refractory hypoxemia after cardiothoracic surgery.

BACKGROUND: The purpose of this study was to describe our institutional experience in using inhaled prostacyclin as a selective pulmonary vasodilator in patients with pulmonary hypertension, refractory hypoxemia, and right heart dysfunction after cardiothoracic surgery. METHODS: Between February 2001 and March 2003, cardiothoracic surgical patients with pulmonary hypertension (mean pulmonary artery pressure >30 mm Hg or systolic pulmonary artery pressure >40 mm Hg), hypoxemia (PaO(2)/fraction of inspired oxygen <150 mm Hg), or right heart dysfunction (central venous pressure >16 mm Hg and cardiac index <2.2 L.min(-1).m(-2)) were prospectively administered inhaled prostacyclin at an initial concentration of 20,000 ng/mL and then weaned per protocol. Hemodynamic variables were measured before the initiation of inhaled prostacyclin, 30 to 60 minutes after initiation, and again 4 to 6 hours later. RESULTS: One hundred twenty-six patients were enrolled during the study period. At both time points, inhaled prostacyclin significantly decreased the mean pulmonary artery pressure without altering the mean arterial pressure. The average length of time on inhaled prostacyclin was 45.6 hours. There were no adverse events attributable to inhaled prostacyclin. The average cost for inhaled prostacyclin was 150 US dollars per day. Compared with nitric oxide, which costs 3000 US dollars per day, the potential cost savings over this period were 681,686 US dollars. CONCLUSIONS: Inhaled prostacyclin seems to be a safe and effective pulmonary vasodilator for cardiothoracic surgical patients with pulmonary hypertension, refractory hypoxemia, or right heart dysfunction. Overall, inhaled prostacyclin significantly decreases mean pulmonary artery pressures without altering the mean arterial pressure. Compared with nitric oxide, there is no special equipment required for administration or toxicity monitoring, and the cost savings are substantial.

Perspective: Hospital support for anesthesiology departments: aligning incentives and improving productivity.

Anesthesiology groups, particularly academic departments, are increasingly dependent on hospital support for financial viability. Economic stresses are driven by higher patient acuity, by multiple subspecialty service and call demands, by high-risk obstetric services, and by long case durations attributable to both case complexity and time for teaching. An unfavorable payer mix, university taxation, and other costs associated with academic education and research missions further compound these stresses. In addition, the current economic climate and the uncertainty surrounding health care reform measures will continue to increase performance pressures on hospitals and anesthesiology departments.Although many researchers have published on the mechanics of operating room (OR) productivity, their investigations do not usually address the motivational forces that drive individual and group behaviors. Institutional tradition, surgical convenience, and parochial interests continue to play predominant roles in OR governance and scheduling practices. Efforts to redefine traditional relationships, to coordinate operational decision-making processes, and to craft incentives that align individual performance goals with those of the institution are all essential for creating greater economic stability. Using the principles of shared costs, department autonomy, hospital flexibility and control over institutional issues, and alignment between individual and institutional goals, the authors developed a template to redefine the hospital-anesthesiology department relationship. Here, they describe both this contractual template and the results that followed implementation (2007-2009) at one institution.

Impact of pulmonary hypertension on outcomes after aortic valve replacement for aortic valve stenosis.

OBJECTIVE: The presence of pulmonary hypertension historically has been considered a significant risk factor affecting early and late outcomes after valve replacement. Given the number of recent advances in the management of pulmonary hypertension after cardiac surgery, a better understanding of its impact on outcomes may assist in the clinical management of these patients. The purpose of this study was to determine whether pulmonary hypertension remains a risk factor in the modern era for adverse outcomes after aortic valve replacement for aortic valve stenosis. METHODS: From January 1996 to June 2009, a total of 1080 patients underwent aortic valve replacement for primary aortic valve stenosis, of whom 574 (53%) had normal systolic pulmonary artery pressures (sPAP) and 506 (47%) had pulmonary hypertension. Pulmonary hypertension was defined as mild (sPAP 35-44 mm Hg), moderate (45-59 mm Hg), or severe (≥ 60 mm Hg). In the group of patients with pulmonary hypertension, 204 had postoperative echocardiograms. RESULTS: Operative mortality was significantly higher in patients with pulmonary hypertension (47/506, 9%, vs 31/574, 5%, P = .02). The incidence of postoperative stroke was similar (P = .14), but patients with pulmonary hypertension had an increased median hospital length of stay (8 vs 7 days, P = .001) and an increased incidence of prolonged ventilation (26% vs 17%, P < .001). Preoperative pulmonary hypertension was an independent risk factor for decreased long-term survival (relative risk 1.7, P = .02). Those with persistent pulmonary hypertension postoperatively had decreased survival. Five-year survival (Kaplan-Meier) was 78% ± 6% with normal sPAP and 77% ± 7% with mild pulmonary hypertension postoperatively, compared with 64% ± 8% with moderate and 45% ± 12% with severe pulmonary hypertension (P < .001). CONCLUSIONS: In patients undergoing aortic valve replacement, preoperative pulmonary hypertension increased operative mortality and decreased long-term survival. Patients with persistent moderate or severe pulmonary hypertension after aortic valve replacement had decreased long-term survival. These data suggest that pulmonary hypertension had a significant impact on outcomes in patients undergoing aortic valve replacement and should be considered in preoperative risk assessment.

Mild hypercapnia after uncomplicated heart surgery is not associated with hemodynamic compromise.

OBJECTIVE: The aim of this study was to examine the effects of small changes in PaCO(2) on hemodynamic parameters after uncomplicated heart surgery with cardiopulmonary bypass. DESIGN: This was a prospective, randomized crossover study. SETTING: A large academic medical center. PARTICIPANTS: Twenty-four subjects who were scheduled for elective cardiac surgery were enrolled in this study. INTERVENTIONS: Each subject underwent the normal procedures that are associated with cardiac surgery. General anesthesia, including muscle relaxation, were continued in the immediate postoperative period. Measured tidal volumes and minute ventilation were kept constant for the duration of the study. Target PaCO(2) concentrations of 30, 40, and 50 mmHg were achieved by adding varying amounts of exogenous CO(2) gas to the inhaled oxygen. Various measurements were made at each target PaCO(2), including cardiac index, mixed venous oxygen saturation, blood pressure, heart rate, and pulmonary artery pressure. MEASUREMENTS AND MAIN RESULTS: Twenty-four patients were enrolled. Seven were withdrawn before commencement of the study. The cardiac index increased when the PaCO(2) was increased from 30 to 40 mmHg (p < 0.001) and remained unchanged between 40 and 50 mmHg. Mixed venous oxygen saturation increased (p < 0.001) with elevations in PaCO(2) up to 50 mmHg and decreased again when the PaCO(2) was returned to 30 mmHg. The blood pressure decreased (p < 0.001) with increasing PaCO(2). The pulmonary pressure increased (p < 0.001) with elevations in PaCO(2). No patient became hemodynamically unstable or had any arrhythmias. CONCLUSION: The findings of this study suggest that unless there is a specific contraindication to mild hypercapnia, such as pulmonary hypertension or hemodynamic instability, concerns about mild respiratory acidosis should not prevent weaning of sedation and mechanical ventilation after uncomplicated heart surgery.

Neutrophils and neutrophil products do not mediate pulmonary hemodynamic effects of endotoxin on oleic acid-induced lung injury.

UNLABELLED: Small-dose endotoxin (Etx) prevents pulmonary perfusion redistribution away from edematous dorsal lung regions after oleic acid (OA)-induced injury in dogs, causing a significant deterioration in oxygenation. We hypothesized that small-dose Etx might mediate this effect via polymorphonuclear neutrophil (PMN) priming with release of inflammatory mediators such as platelet activating factor (PAF) or secretory phospholipase A(2) (sPLA(2)). To test this hypothesis, we administered specific inhibitors directed against each mediator and used two strategies to generate neutropenia. PAF and sPLA(2) inhibitors were administered before OA injury, followed 2 h later by small-dose Etx (n = 4 each group). PMN depletion was achieved by hydroxyurea administration for 5 days before the study to achieve absolute neutrophil counts <1000/mm(3) (n = 4). Inhibition of PMN adherence to lung endothelium was achieved by the administration of an anti-CD18 monoclonal antibody immediately before lung injury (n = 5). Positron emission tomography was used to evaluate pulmonary perfusion distribution and lung water content. We observed no effect of these interventions on the perfusion pattern after Etx + OA. Thus, neither neutrophils nor PAF or sPLA(2) mediate the effects of Etx on the pattern of perfusion in this model of lung injury. IMPLICATIONS: Acute respiratory failure is characterized by severe decreases in blood oxygen. The pattern of blood flow within the lungs can contribute to this problem. This study investigated the potential role of white blood cells and their products in mediating abnormal pulmonary blood flow patterns in an experimental animal model of respiratory failure.